The prevailing model of physical injury indicates the primary traumatic agent in injury is the transfer of energy in amounts exceeding local tissue thresholds. Of interest for the present study is mechanical energy transfer in vocal fold (VF) injury during phonation. One important source of such injury is perpendicular VF impact stress (force/area), which in turn is partially regulated by VF adduction and phonatory subglottal pressure (PS) [32, 33]. A gap in the literature, which this project addresses, regards the effects of high respiratory drive (HRD) - i.e., increased ventilation due to blood-gas level changes during aerobic activity [1] - on adduction and PS, and thus VF injury risk in human subjects. Of particular interest are individuals required to phonate loudly during aerobic activity (HRD), such as military drill instructors, firefighters, physical education teachers, and others. Existing data indicate that when voice output is free to vary under HRD, expiratory flow increases [22, 24], presumably in conjunction with relatively abducted vocal folds. Thus, the risk of injury should be minimal. However, data indicate individuals in the foregoing occupations actually have elevated risk for phonotrauma [2-12], which is thought to be associated with increased VF adduction, PS and impact stress. The general hypothesis pursued in this study is that in a laboratory setting requiring loud voice during HRD, VF adduction as well as estimated PS will increase rather than decrease, thus increasing the risk of VF injury. Further, respiratory homeostasis (maintenance of optimum blood-gas concentrations), as measured by minute ventilation and blood-gas levels, will be compromised in that scenario. Conversely, when voice output is free to vary under HRD, respiratory homeostasis will be better preserved, but voice output will be compromised, as measured by decreased adduction and PS, thus decreasing injury risk. Stated differently, this project investigates a proposed competition between the vocal folds' function as a gateway to blood-gas regulation versus oscillating sound source. The study utilizes a physiologic stressor, aerobic exercise, to investigate laryngeal behavior during HRD as a window into the mechanisms of phonotrauma in physically active voice users. Specific Aims are: SA 1: To investigate the influence of (a) vocal goal and (b) exercise workload on respiratory function. The hypothesis is that loud phonation will disproportionately interfere with ventilatory homeostasis during an aerobic exercise challenge as compared with spontaneous phonation. SA 2: To investigate the influence of (a) vocal goal and (b) exercise workload on laryngeal function. The hypothesis is that with increasing HRD, loud phonation will result in a disproportional increase in VF adduction and estimated PS, and thus injury risk, compared to spontaneous phonation. The project's significance lies with its investigation of mechanisms of VF injury in general and of occupationally induced VF injury associated with HRD in particular. PUBLIC HEALTH RELEVANCE: The proposed research will characterize the effects of aerobic activity, a physiologic stressor, and vocal goal on respiratory and laryngeal function using non-invasive measures in human subjects. The knowledge gained from this research will guide the development of future large-scale clinical studies to elucidate the effects of different approaches to vocal and cardiorespiratory training in the rehabilitation of physically active voice users with voice problems.